Search results for "tumorigenesis"

showing 10 items of 15 documents

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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[How some commensal bacteria would exacerbate colorectal carcinogenesis?].

2016

International audience; The gut microbiota maintains a relationship with its host with strong mutual benefits. Changes in the composition of the intestinal microbiota have been detected in colorectal cancer patients to the extent that it is now considered as a real contributing factor in this pathology. In this review, we focus on three commensal bacterial species, namely Bacteroides fragilis, Fusobacterium nucleatum, and Escherichia coli, which seem to emerge as pathogens and to contribute to colorectal carcinogenesis through their inflammatory and oncogenic properties.; Le microbiote intestinal entretient une relation mutualiste forte avec l’hôte. Depuis la mise en évidence de modificatio…

0301 basic medicineColorectal cancer[SDV]Life Sciences [q-bio]enterotoxigenic bacteroides-fragilis[SDV.CAN]Life Sciences [q-bio]/Cancer[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyGut floradnamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biology[ SDV.CAN ] Life Sciences [q-bio]/CancerMicrobiology03 medical and health sciences0302 clinical medicine[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineEscherichia colimucosatumorisgenesisComputingMilieux_MISCELLANEOUSGastrointestinal tract[ SDV ] Life Sciences [q-bio]biologyfusobacterium-nucleatumHost (biology)General Medicinebiology.organism_classificationmedicine.disease[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriologymicroenvironment3. Good healthstomatognathic diseasestumorigenesis030104 developmental biologyinflammation030220 oncology & carcinogenesisgutcellsBacteroides fragilisFusobacterium nucleatumCarcinogenesiscolon-cancer[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Silencing of hepatic fate-conversion factors induce tumorigenesis in reprogrammed hepatic progenitor-like cells

2016

Abstract Background Several studies have reported the direct conversion of mouse fibroblasts to hepatocyte-like cells with different degrees of maturation by expression of hepatic fate-conversion factors. Methods We have used a combination of lentiviral vectors expressing hepatic fate-conversion factors with Oct4, Sox2, Klf4, and Myc to convert mouse embryonic fibroblasts into hepatic cells. Results We have generated hepatic cells with progenitor-like features (iHepL cells). iHepL cells displayed basic hepatocyte functions but failed to perform functions characteristic of mature hepatocytes such as significant Cyp450 or urea cycle activities. iHepL cells expressed multiple hepatic-specific …

0301 basic medicineMaleCarcinogenesisCellular differentiationMedicine (miscellaneous)Gene ExpressionReceptors G-Protein-CoupledMiceMice Inbred NODHepatocyteTransgenesStem CellsTeratomaCell DifferentiationForkhead Transcription FactorsCellular ReprogrammingCell biologyKLF4Molecular MedicineStem cellReprogrammingDirect reprogrammingGenetic VectorsKruppel-Like Transcription FactorsBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Proto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4SOX2AnimalsHepatectomyGene SilencingProgenitor cellResearchXenograftSOXB1 Transcription FactorsLentivirusCD24 AntigenCell BiologyFibroblastsEmbryo MammalianEmbryonic stem cell030104 developmental biologyTumorigenesisHepatic stellate cellHepatocytesOctamer Transcription Factor-3BiomarkersProgenitorStem Cell Research & Therapy
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DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
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Deciphering genomic heterogeneity and the internal composition of tumour activities through a hierarchical factorisation model

2021

Genomic heterogeneity constitutes one of the most distinctive features of cancer diseases, limiting the efficacy and availability of medical treatments. Tumorigenesis emerges as a strongly stochastic process, producing a variable landscape of genomic configurations. In this context, matrix factorisation techniques represent a suitable approach for modelling such complex patterns of variability. In this work, we present a hierarchical factorisation model conceived from a systems biology point of view. The model integrates the topology of molecular pathways, allowing to simultaneously factorise genes and pathways activity matrices. The protocol was evaluated by using simulations, showing a hi…

:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]Matrix factorisationComputer scienceBioinformaticsGeneral MathematicsSystems biologyPopulationMatrix factorisationContext (language use)Computational biologyComputational biologyGenomic heterogeneitygenomic heterogeneityFactorizationBioinformàticaSimulació per ordinadorComputer Science (miscellaneous)QA1-939cancerVariabilityeducationEngineering (miscellaneous)Topology (chemistry)Cancereducation.field_of_studyvariabilitymatrix factorisationLimitingbioinformaticsCàncer--Aspectes genèticsGenòmicaBreast--CancerTumorigenesisMathematics
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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Classification or non-classification of substances with positive tumor findings in animal studies: Guidance by the German MAK commission

2019

One of the important tasks of the German Senate Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area (known as the MAK Commission) is in the evaluation of a potential for carcinogenicity of hazardous substances at the workplace. Often, this evaluation is critically based on data on carcinogenic responses seen in animal studies and, if positive tumor responses have been observed, this will mostly lead to a classification of the substance under investigation into one of the classes for carcinogens. However, there are cases where it can be demonstrated with a very high degree of confidence that the tumor findings in the experimental animals are not relevant…

Life sciences; biologyApplied psychologyMechanism of tumorigenesisGuidelines as TopicCommissionAir Pollutants Occupational010501 environmental sciencesToxicology030226 pharmacology & pharmacy01 natural sciencesRisk AssessmentGerman03 medical and health sciences0302 clinical medicineGovernment AgenciesSpecies SpecificityTumor Findingsddc:570GermanyNeoplasmsOccupational ExposureAnimalsHumansHuman relevance0105 earth and related environmental sciencesCarcinogenicitySpecies-specific tumorsMaximally tolerated doseInternational AgenciesGeneral Medicinelanguage.human_languageOccupational DiseasesCategorizationlanguageCarcinogensDegree of confidencePsychologyAnimal tumor studiesOrgan-specific tumors
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Cell Systems Bioelectricity: How Different Intercellular Gap Junctions Could Regionalize a Multicellular Aggregate

2021

Simple Summary Electric potential patterns across tissues are instructive for development, regeneration, and tumorigenesis because they can influence transcription, migration, and differentiation through biochemical and biomechanical downstream processes. Determining the origins of the spatial domains of distinct potential, which in turn decide anatomical features such as limbs, eyes, brain, and heart, is critical to a mature understanding of how bioelectric signaling drives morphogenesis. We studied theoretically how connexin proteins with different voltage-gated gap junction conductances can maintain multicellular regions at distinct membrane potentials. We analyzed a minimal model that i…

Membrane potentialCancer ResearchChemistryelectric potential patternsCellGap junctioncell bioelectricityConnexinNeoplasms. Tumors. Oncology. Including cancer and carcinogension channelsArticleMulticellular organismtumorigenesismedicine.anatomical_structureElectrical SynapsesOncologyEvolutionary developmental biologymedicineintercellular gap junctionsNeuroscienceIon channelRC254-282Cancers
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miR-205-5p-mediated downregulation of ErbB/HER receptors in breast cancer stem cells results in targeted therapy resistance

2015

AbstractThe ErbB tyrosine kinase receptor family has been shown to have an important role in tumorigenesis, and the expression of its receptor members is frequently deregulated in many types of solid tumors. Various drugs targeting these receptors have been approved for cancer treatment. Particularly, in breast cancer, anti-Her2/EGFR molecules represent the standard therapy for Her2-positive malignancies. However, in a number of cases, the tumor relapses or progresses thus suggesting that not all cancer cells have been targeted. One possibility is that a subset of cells capable of regenerating the tumor, such as cancer stem cells (CSCs), may not respond to these therapeutic agents. Accumula…

P63cancer stem cellsCancer ResearchReceptor ErbB-2oncogenesmedicine.medical_treatmentmedicine.disease_causeTargeted therapyERBB3Molecular Targeted TherapyDEATHErbB ReceptorsGene Expression Regulation NeoplasticNeoplastic Stem CellsFemaleOriginal Articlemedicine.drugCARCINOMAMIGRATIONCancer Stem Cells; Breast CancerImmunologyBreast NeoplasmsCancer Stem CellMIR-205miR-205-5pBiologyLapatinibcancer treatmentNOCellular and Molecular Neurosciencebreast cancerBreast cancerErbBCancer stem cellCell Line TumormedicineHumansSUPPRESSIONCell ProliferationMESENCHYMAL TRANSITIONtumorigenesis cancer treatment cancer stem cells miR-205-5p oncogenes breast cancerMICRORNA EXPRESSIONTumor Suppressor ProteinsLapatinibCell BiologyTrastuzumabmedicine.diseaseGENEMicroRNAstumorigenesisDrug Resistance NeoplasmCancer cellQuinazolinesCancer researchNeoplasm Recurrence LocalCarcinogenesisTranscription FactorsCell Death & Disease
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Molecular Mechanisms Leading from Periodontal Disease to Cancer

2022

Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axi…

QH301-705.5periodontal diseaseReviewOdontologi<i>Porphyromonas gingivalis</i>Catalysisimmune responseInorganic ChemistrycancerHumansBiology (General)Physical and Theoretical ChemistryImmune responseQD1-999Molecular BiologySpectroscopyPeriodontal DiseasesCancerCancer och onkologiRANK ligandFusobacterium nucleatumReceptor Activator of Nuclear Factor-kappa B<i>Fusobacterium nucleatum</i>Organic ChemistryGeneral MedicineComputer Science ApplicationsChemistrytumorigenesisGene Expression RegulationDentistryCancer and OncologyTumorigenesisDisease ProgressionCytokinesMouth NeoplasmsPeriodontal diseasePorphyromonas gingivalisSignal Transduction
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